The heterozygous mutation of mouse ANKRD11 caused a decreased cortical precursor proliferation and perturbed genesis of neurons, leading to the increase of HDAC3‐regulated H4K5ac, H4K8ac, H3K9ac, and H4K16ac.[24a] The phenotype of biallelic 65K/RNPC3 variants is mainly associated with growth hormone deficiency, delayed bone, intellectual disability, and brain anomalies.[44] We also searched human cancer data (GEPIA2 database), and found that the expression of Hs65K, HsANKRD11, and HDAC3 is significantly changed in tumors versus normal tissues (Figure S8E, Supporting Information). This evidence concerns the gene RNPC3 and Intellectual disability.